title: Aging, age-related diseases and peroxisomes.
abstract: Human aging is considered as one of the biggest risk factors for the development of multiple diseases such as cancer, type-2 diabetes, and neurodegeneration. In addition, it is widely accepted that these age-related diseases result from a combination of various genetic, lifestyle, and environmental factors. As biological aging is a complex and multifactorial phenomenon, the molecular mechanisms underlying disease initiation and progression are not yet fully understood. However, a significant amount of evidence supports the theory that oxidative stress may act as a primary etiologic factor. Indeed, many signaling components like kinases, phosphatases, and transcription factors are exquisitely sensitive to the cellular redox status, and a chronic or severe disturbance in redox homeostasis can promote cell proliferation or trigger cell death. Now, almost 50 years after their discovery, there is a wealth of evidence that peroxisomes can function as a subcellular source, sink, or target of reactive oxygen and nitrogen molecules. Yet, the possibility that these organelles may act as a signaling platform for a variety of age-related processes has so far been underestimated and largely neglected. In this review, we will critically discuss the possible role of peroxisomes in the human aging process in light of the available data.
authors.affiliation: Department of Cellular and Molecular Medicine, KU Leuven, Herestraat 49, 601, B-3000, Leuven, Belgium, marc.fransen@med.kuleuven.be.
authors.forename: Marc
authors.initials: M
authors.lastname: Fransen
authors.forename: Marcus
authors.initials: M
authors.lastname: Nordgren
authors.forename: Bo
authors.initials: B
authors.lastname: Wang
authors.forename: Oksana
authors.initials: O
authors.lastname: Apanasets
authors.forename: Paul P
authors.initials: PP
authors.lastname: Van Veldhoven
mesh_terms: D000367:Age Factors; D000375:Aging / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D009369:Neoplasms / Q000378:metabolism* / Q000473:pathology; D019636:Neurodegenerative Diseases / Q000378:metabolism* / Q000473:pathology; D010084:Oxidation-Reduction; D020675:Peroxisomes / Q000378:metabolism* / Q000473:pathology; D015398:Signal Transduction